Serum from Reye's Syndrome patients has been shown to disrupt respiratory function and morphology in isolated rat liver mitochondria. The results suggested the existence of a serum factor that may be important in the pathogenesis of Reye's Syndrome. To further define pathophysiologial role for the serum factor, we propose to explore the mechanism of action of the factor at the level of the electron transport chain in isolated mitochondria, and also to masure the effects of patient serum on energy-linked functions in isolated liver cells. The cellular metabolic functions of interest include; fatty acid oxidation, urea synthesis, protein synthesis, and cellular respiration, all of which are relevant to the symptoms of Reye's Syndrome. Meanwhile we will continue efforts to determine the chemical identify of the serum factor using micro-purification techniques and mass spectrometry. In addition to the biochemical studies we plan to assay the serum of Reye's patients, parents, siblings, and viral-illness control patients for the serum factor, SGOT, prothrombin time, and NH3. This will further define the specificity of the serum factor for Reye's Syndrome, and may suggest answers to questions of genetic susceptibility versus environmental causes. The results will also be used to evaluate the potential use of the bio-assay for serum factor as an innovative diagnostic tool.